PMID- 29990865
OWN - NLM
STAT- MEDLINE
DCOM- 20181218
LR  - 20181218
IS  - 1950-6007 (Electronic)
IS  - 0753-3322 (Linking)
VI  - 106
DP  - 2018 Oct
TI  - Tangganjian decoction ameliorates type 2 diabetes mellitus and nonalcoholic fatty 
      liver disease in rats by activating the IRS/PI3K/AKT signaling pathway.
PG  - 733-737
LID - S0753-3322(18)30977-6 [pii]
LID - 10.1016/j.biopha.2018.06.089 [doi]
AB  - AIM: Previous clinical studies have demonstrated that tangganjian (TGJ), a modern 
      Chinese prescribed medicine, has a clinical effect in the treatment of type 2 
      diabetes mellitus (T2DM) with nonalcoholic fatty liver disease (NAFLD). Our study 
      aimed to investigate whether the phosphatidylinositol 3-kinase (PI3K)/protein 
      kinase B (AKT) signaling pathway is involved in this therapeutic effect. 
      MATERIALS AND METHODS: T2DM and NAFLD rat models were constructed and treated 
      with three different concentrations of TGJ. Pioglitazone was used as a positive 
      control, along with the model and normal groups. For analyses, blood and livers 
      were collected. Levels of glucose and lipid metabolism indicators, including 
      fasting insulin and total cholesterol, were determined. The expression levels of 
      insulin receptor substrate (IRS), PI3K, and AKT were also determined by western 
      blotting and immunohistochemistry. Liver tissues were stained with hematoxylin & 
      eosin. RESULTS: In the high-dose TGJ-treated and positive groups, there was a 
      significant increase in the HDL-C level and decreases in the levels of the 
      fasting blood glucose, 2 h postprandial blood glucose, fasting insulin, 
      triglyceride, total cholesterol, and low-density lipoprotein cholesterol, along 
      with a significant increase in the expression of IRS, PI3K, and AKT in the liver. 
      TGJ could also attenuate or counteract the effects of T2DM and NAFLD in the liver 
      lobules. CONCLUSION: A high concentration of TGJ can improve glucose and lipid 
      metabolism by activating the IRS/PI3K/AKT signaling pathway.
CI  - Copyright (c) 2018 Elsevier Masson SAS. All rights reserved.
FAU - Fan, Yanbo
AU  - Fan Y
AD  - Science and Education Department, Wuhan Hospital of Traditional Chinese Medicine, 
      Wuhan, Hubei 430014, PR China; Post-doctoral Research Center of Mayinglong 
      Pharmaceutical Group Co., Ltd., Wuhan, Hubei 430060, PR China.
FAU - He, Zhiwei
AU  - He Z
AD  - Department of pharmacy, Xiangyang Hospital of Traditional Chinese Medicine, 
      Xiangyang, Hubei 441099, PR China.
FAU - Wang, Wei
AU  - Wang W
AD  - Department of Pharmacy, Wuhan Hospital of Traditional Chinese Medicine, Wuhan, 
      Hubei 430014, PR China.
FAU - Li, Jingjing
AU  - Li J
AD  - College of Basic Medicine, Hubei University of Chinese Medicine, Wuhan, Hubei 
      430065, PR China.
FAU - Hu, Aimin
AU  - Hu A
AD  - Endocrinology Department, Wuhan Hospital of Traditional Chinese Medicine, Wuhan, 
      Hubei 430014, PR China.
FAU - Li, Li
AU  - Li L
AD  - Department of Pharmacy, Wuhan Hospital of Traditional Chinese Medicine, Wuhan, 
      Hubei 430014, PR China.
FAU - Yan, Ling
AU  - Yan L
AD  - Endocrinology Department, Wuhan Hospital of Traditional Chinese Medicine, Wuhan, 
      Hubei 430014, PR China.
FAU - Li, Zhijie
AU  - Li Z
AD  - Department of Encephalopathy, Wuhan Hospital of Traditional Chinese Medicine, 
      Wuhan, Hubei 430014, PR China.
FAU - Yin, Qiang
AU  - Yin Q
AD  - Department of Management, Xinjiang Uygur Pharmaceutical Co., Ltd., Wulumuqi, 
      Xinjiang 830001, PR China. Electronic address: qiangy_0405@163.com.
LA  - eng
PT  - Journal Article
DEP - 20180711
PL  - France
TA  - Biomed Pharmacother
JT  - Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie
JID - 8213295
RN  - 0 (Biomarkers)
RN  - 0 (Blood Glucose)
RN  - 0 (Dietary Sugars)
RN  - 0 (Drugs, Chinese Herbal)
RN  - 0 (Hypoglycemic Agents)
RN  - 0 (Hypolipidemic Agents)
RN  - 0 (Insulin)
RN  - 0 (Insulin Receptor Substrate Proteins)
RN  - 0 (Lipids)
RN  - 5W494URQ81 (Streptozocin)
RN  - EC 2.7.1.137 (Phosphatidylinositol 3-Kinase)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
SB  - IM
MH  - Animals
MH  - Biomarkers/blood
MH  - Blood Glucose/*drug effects/metabolism
MH  - Diabetes Mellitus, Experimental/blood/*drug therapy/enzymology/etiology
MH  - Diabetes Mellitus, Type 2/blood/*drug therapy/enzymology/etiology
MH  - Diet, High-Fat
MH  - Dietary Sugars
MH  - Dose-Response Relationship, Drug
MH  - Drugs, Chinese Herbal/*pharmacology
MH  - Dyslipidemias/blood/drug therapy/enzymology
MH  - Hypoglycemic Agents/*pharmacology
MH  - Hypolipidemic Agents/*pharmacology
MH  - Insulin/blood
MH  - Insulin Receptor Substrate Proteins/*metabolism
MH  - Lipids/blood
MH  - Liver/*drug effects/enzymology/pathology
MH  - Male
MH  - Non-alcoholic Fatty Liver Disease/blood/*drug therapy/enzymology/etiology
MH  - Phosphatidylinositol 3-Kinase/*metabolism
MH  - Proto-Oncogene Proteins c-akt/*metabolism
MH  - Rats, Wistar
MH  - Signal Transduction/drug effects
MH  - Streptozocin
OTO - NOTNLM
OT  - IRS/PI3K/AKT signaling pathway
OT  - Nonalcoholic fatty liver disease
OT  - Tangganjian
OT  - Type 2 diabetes mellitus
OT  - Wistar rats
EDAT- 2018/07/11 06:00
MHDA- 2018/12/19 06:00
CRDT- 2018/07/11 06:00
PHST- 2018/02/10 00:00 [received]
PHST- 2018/06/14 00:00 [revised]
PHST- 2018/06/14 00:00 [accepted]
PHST- 2018/07/11 06:00 [pubmed]
PHST- 2018/12/19 06:00 [medline]
PHST- 2018/07/11 06:00 [entrez]
AID - S0753-3322(18)30977-6 [pii]
AID - 10.1016/j.biopha.2018.06.089 [doi]
PST - ppublish
SO  - Biomed Pharmacother. 2018 Oct;106:733-737. doi: 10.1016/j.biopha.2018.06.089. 
      Epub 2018 Jul 11.